Modulation of the immune response by a methanol-insoluble fraction of attenuated tubercle bacilli (bcg). II. Relationship of antigen dose to heightened primary and secondary immune responses to sheep red blood cells.

A methanol extraction residue (MER) of BCG has previously been shown to heighten host resistance to a subsequent challenge with microorganisms or syngeneic tumour grafts and to stimulate the antibody response to sheep red blood cells (SRBC) and phage T(2). Present investigations on the effect of antigen dose on MER stimulation of the primary and secondary response to SRBC indicated that: (1) Pretreatment by MER stimulates the early primary response most effectively when the immunizing dose of SRBC is less than maximum, and this is due to a greater increase by MER of 19S antibody with low doses of antigen than with high doses of SRBC. Maximum 7S antibody production is higher in MER treated animals at all antigen doses. (2) MER administered after low doses of SRBC but not high doses stimulates the ongoing primary haemagglutinin response. (3) Maximum secondary responses of mice treated with MER before priming are considerably elevated above the corresponding controls and the secondary responses in treated mice are not inhibited by high priming doses of antigen. These results are discussed in relation to the locus of MER activity

Mutations affecting uridine monophosphate pyrophosphorylase or the argR gene in Escherichia coli - Effects on carbamoyl phosphate and pyrimidine biosynthesis and on uracil uptake

In the course of experiments directed towards the isolation of mutants of Escherichia coli K12 with altered regulation of the synthesis of carbamoylphosphate synthetase, two types of mutations were found to affect the cumulative repression of this enzyme by arginine and uracil. Alteraction of the arginine pathway regulatory gene, argR, was shown to reduce the repressibility of the enzyme by both end products while mutations affecting uridine monophosphate pyrophosphorylase (upp) besides affecting uracil uptake preclude enzyme repression by uracil or cytosine in the biosynthesis of carbamoylphosphate and the pyrimidines. The upp mutations were located on the chromosome near the gua operon. Mutations previously designated as uraP are shown to belong to this class. The relation that could exist between the loss of uridine monophosphate pyrophosphorylase and the impairment of uracil uptake is discussed. A new method for isolating argR mutants in arginine-less strains is described. © 1972 Springer-Verlag.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Characterization of IgM and IgG Antibodies Produced During the Anamnestic Response Initiated In Vitro

Rabbit lymph node fragments undergoing an anamnestic response in vitro produce both 7 S (IgG) and 19 S (IgM) antibodies as well as inconstant amounts of 28 S antibodies that are presumably of IgM type. The majority of the antibodies produced are of the 7 S type, which, after 15 days of culture, can represent more than 90% to 99% of the antibody activity in the fluids; however, small amounts of 19 S antibodies can be present for up to 15 days in these culture fluids. While the absolute amounts of antibody activity, radioactivity incorporated and protein increased over the course of these experiments, it is inferred that antibody is only a relatively small percentage of the newly synthesized protein that is present in the culture fluids

Nucleotide pool in pho regulon mutants and alkaline phosphatase synthesis in Escherichia coli.

The intracellular nucleotide pool of Escherichia coli W3110 reproducibly changes from conditions of growth in phosphate excess to phosphate starvation, with at least two nucleotides appearing under starvation conditions and two nucleotides appearing only under excess phosphate conditions. Strains bearing a deletion of the phoA gene show the same pattern, indicating that dephosphorylation by alkaline phosphatase is not responsible for the changes. Strains with mutations in the phoU gene, which result in constitutive expression of the pho regulon, show the nucleotide pattern of phosphate-starved cells even during phosphate excess growth. These changes in nucleotides are therefore due to phoU mutation but not to alkaline phosphatase constitutivity. In fact, a phoR (phoR68) mutant strain has the patterns of the wild type in spite of being constitutive for alkaline phosphatase. That these nucleotides might be specific signals for pho regulon expression was supported by the fact that the two nucleotides appearing under phosphate starvation induced the synthesis of alkaline phosphatase in repressed permeabilized wild-type cells under conditions of phosphate excess

Predictors of Early and Late Mortality for Patients with Hematologic Malignancy and Invasive Mold Disease

Background: Invasive mold infections (IMI) are leading infectious causes of mortality among patients with hematological malignancies. Objectives: To determine the relative contribution of host, disease, and treatment-related factors to patient survival. Methods: An observational, retrospective cohort study reviewing the medical records of patients with hematological malignancy and IMI (2006–2016). Causes of death were classified up to 90 days after diagnosis. Kaplan–Meier and Cox regression analyses were used to determine risk factors for early, late, and overall mortality. Results: Eighty-six patients with IMI were included; 29 (34%) and 41 (47%) died within 6 and 12 weeks of diagnosis, respectively. Death was attributed to IMI in 22 (53.6%) patients, all of whom died within 45 days of diagnosis. Risk factors for early mortality were elevated serum galactomannan, treatment with amphotericin B, IMI progression 3 weeks after diagnosis, and lymphoma undergoing HCT. Late mortality was associated with relapsed/refractory malignancy and elevated serum galactomannan. Conclusions: In this single-center study of patients with IMI, infections were the most frequent causes of death, and time-dependent risk factors for death were identified. These results may help direct risk-assessment and monitoring of patients undergoing treatment of IMI